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ROSI was also able to reduce thyrocyte growth by 40% in a murine knock-in model of thyroid hormone receptor β [ 107].
During this research, a model of thyroid carcinoma progression based on genome-wide expression datasets has been built by using three different approaches and two validation sets.
This observational study demonstrates the recovery of thyroid morphology as seen on sonography after treating patients according to the principles of the WOMED model of thyroid disease.
Src activity has been observed to be elevated in a murine model of thyroid cancer, and hyper-activation of Src is associated with HIF activity, at least in this model (20).
We recently identified mutations in two mitochondrial DNA-encoded subunits resulting in severe loss of mitochondrial activity in a cell model of thyroid oncocytic tumours (Bonora et al, 2006).
However, activation of AMPK has also been associated with increased GLUT1 expression in a rat model of thyroid cells, and increased glucose uptake in thyroid cancer cells has been linked to thyroid cancer progression and aggressiveness [ 24– 26].
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Lu, C., Willingham, M. C., Furuya, F. & Cheng, S. Y. Activation of phosphatidylinositol 3-kinase signaling promotes aberrant pituitary growth in a mouse model of thyroid-stimulating hormone-secreting pituitary tumors.
This is the basic assumption that we have included in the musculoskeletal model of thyroid-associated orbitopathy [76].
In this study, by using in vivo and ex vivo experimental models of thyroid cancer we show the possibility to obtain a reliable thyroid cancer imaging in vivo by targeting the galectin-3 lectin molecule.
Rodent models of thyroid system dysfunction were presented.
Therefore, the analysis of the experimental models of thyroid carcinogenesis seems to confirm that the UbcH10 overexpression is essentially restricted to the undifferentiated histotype.
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